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Una D Mccann - One of the best experts on this subject based on the ideXlab platform.
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Pentagastrin induced sleep panic attacks panic in the absence of elevated baseline arousal
Biological Psychiatry, 2002Co-Authors: Marilla Geraci, Robert M Post, Todd S Anderson, Shiyoko Slatecothren, Una D MccannAbstract:Abstract Background It has been suggested that pharmacological challenges that induce panic attacks are confounded by effects of environmental stress, elevated baseline arousal, and expectancy bias. Methods To control for effects of arousal and cognition on the panicogenic effects of Pentagastrin, pharmacological challenges were conducted during sleep in seven patients with panic disorder or social phobia. All patients had previously experienced Pentagastrin-induced panic while awake. Infusions of normal saline and Pentagastrin (0.6 μg/kg) were administered in fixed order and timed so that Pentagastrin infusions took place during the transition from Stage 2 to Stage 3 sleep. Long intravenous lines were placed for remote blood sampling and subsequent analysis of plasma adrenocorticotropic hormone and cortisol. Measures of anxiety and panic were obtained at baseline and upon awakening after pharmacological challenge. Results All seven subjects awoke within seconds following Pentagastrin infusion. Four patients reported symptoms that met criteria for panic. Neither baseline anxiety nor neuroendocrine measures were predictive of panic. Conclusions These data demonstrate the ability to induce panic during a period of diminishing arousal and indicate that panic attacks can occur in the absence of elevated arousal and environmental stress.
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effects of the 5 ht3 antagonist ondansetron on the behavioral and physiological effects of Pentagastrin in patients with panic disorder and social phobia
Neuropsychopharmacology, 1997Co-Authors: Una D Mccann, Christina M Morgan, Marilla Geraci, Shiyoko O Slate, Dennis L Murphy, Robert M PostAbstract:Pentagastrin, a cholecystokinin (CCK) agonist, produces anxiety and panic in patients with panic disorder and social phobia. Preclinical data suggests that Pentagastrin-induced anxiogenesis may be mediated via 5-HT3 receptors. In the present study, 14 patients with panic disorder or social phobia underwent pharmacological challenge in three conditions: (1) pretreatment with saline followed by Pentagastrin infusion; (2) pretreatment with ondansetron followed by Pentagastrin infusion; and (3) pretreatment with saline followed by saline infusion. As expected, Pentagastrin administration led to increased anxiety, physical symptoms of panic attacks, pulse, plasma adrenocorticotropic hormone (ACTH), and cortisol. Pentagastrin's behavioral effects were not blocked by ondansetron, and in fact, tended to be exaggerated. Ondansetron pretreatment did not alter the Pentagastrininduced cortisol increase but significantly prolonged the Pentagastrin-induced increase in ACTH. These findings suggest that Pentagastrin's behavioral effects are not mediated by 5HT3 receptors. Mechanisms by which peripherally administered CCK agonists lead to anxiety remain to be elucidated.
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a comparison of the effects of intravenous Pentagastrin on patients with social phobia panic disorder and healthy controls
Neuropsychopharmacology, 1997Co-Authors: Una D Mccann, Marilla Geraci, Shiyoko O Slate, Diana Roscowterrill, Thomas W UhdeAbstract:The present study sought to determine whether social phobics, like patients with panic disorder, have increased sensitivity to the panicogenic effects of Pentagastrin. Intravenous Pentagastrin and placebo were administered in a double-blind fashion to 19 social phobics, 11 patients with panic disorder, and 19 healthy controls while they participated in a structured social interaction task. Behavioral, cardiovascular, and neuroendocrine responses were obtained. Pentagastrin led to panic attacks in 47% of the social phobics, 64% of the panic disorder patients, and 11% of the healthy controls. The social interaction itself increased anxiety, blood pressure, and pulse in all three groups. These findings suggest that the panicogenic effects of Pentagastrin are not limited to patients with panic disorder and provide further evidence for shared neurobiology in social phobia and panic disorder.
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peptides and anxiety a dose response evaluation of Pentagastrin in healthy volunteers
Anxiety, 1994Co-Authors: Una D Mccann, Marilla Geraci, Shiyoko O Slate, Thomas W UhdeAbstract:A large body of data suggest that brain cholecystokinin (CCK) systems are involved in the regulation of anxiety, and numerous studies have demonstrated that CCK-4, a CCKB agonist, reliably induces panic attacks in patients with panic disorder. Recently, Pentagastrin, a commercially available CCKB agonist, has been reported to have similar anxiogenic properties. To further explore the utility of Pentagastrin as a challenge agent and to determine whether its effects are dose-related, a dose-response study was conducted in ten healthy volunteers. Pentagastrin (0.2 μg kg, 0.6 μg/kg and 1.0 μg/kg) and inactive placebo were infused over one minute on four separate challenge days in a double-blind fashion. Subjects received Pentagastrin while participating in a structured social interaction task. Repeated measures of anxiety, blood pressure, pulse, ACTH, and cortisol were taken at baseline and postinfusion. Pentagastrin administration led to increases in anxiety, pulse, ACTH, cortisol and physical symptoms of panic, in a dose-related manner. Participation in the social interaction task led to increases in measures of anxiety as well as increases in pulse and blood pressure. Few differences were found between the 0.2 μg/kg dose of Pentagastrin and placebo, or between the 0.6 μg/kg and the 1.0 μg/kg doses of Pentagastrin. These findings support the notion that CCK systems are involved in the regulation of anxiety, and suggest that the 0.6 μg/kg dose may be optimal for increasing symptoms of anxiety while minimizing unpleasant side effects. The powerful anxiogenic effects of the social interaction task underscore the importance of contextual variables in challenge studies. Anxiety 1:258–267 (1994/1995). © 1995 Wiley-Liss, Inc.1
Jonathan D Kaunitz - One of the best experts on this subject based on the ideXlab platform.
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Pentagastrin gastroprotection against acid is related to h2 receptor activation but not acid secretion
Gut, 1998Co-Authors: S Tanaka, Y Akiba, Jonathan D KaunitzAbstract:Background —Pentagastrin enhances gastric mucosal defence mechanisms against acid and protects the gastric mucosa from experimental injury. Aims —To investigate whether this gastroprotection is mediated by histamine receptors or occurs as a secondary effect of acid secretion stimulation. Methods —The effects of omeprazole (100 μmol/kg), ranitidine (20 mg/kg), and pyrilamine (10 mg/kg) on Pentagastrin (80 μg/kg/h) induced gastroprotection against acidified aspirin injury were examined in a luminal pH controlled model. The effects of these compounds on Pentagastrin enhanced gastroprotective mechanisms were investigated using intravital microscopy, in which intracellular pH of gastric surface cells (pH i ), mucus gel thickness, gastric mucosal blood flow, and acid output were measured simultaneously. Results —Pentagastrin protected rat gastric mucosa from acidified aspirin injury. This gastroprotection was abolished by ranitidine, but not omeprazole or pyrilamine. Pentagastrin induced a hyperaemic response to luminal acid challenge, increased mucus gel thickness, and elevated pH i during acid challenge. Ranitidine reversed these enhanced defence mechanisms, whereas omeprazole and pyrilamine preserved these effects. Conclusions —These data indicate that Pentagastrin associated gastroprotection and enhanced defence mechanisms against acid result mainly from activation of histamine H 2 receptors, and not as an effect of the stimulation of acid secretion.
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indomethacin does not alter the effect of Pentagastrin on rat gastric defense mechanisms
Peptides, 1996Co-Authors: S Tanaka, Jonathan D KaunitzAbstract:Abstract We studied the effect of the prostaglandin synthesis inhibitor, indomethacin, on Pentagastrin-associated enhancements of gastric mucosal defense mechanisms, using a microfluorometric technique in which mucus gel thickness, intracellular pH (pH i ), gastric mucosal blood flow, and acid secretion were measured simultaneously in vivo. Intravenous infusion with Pentagastrin (80 μg/kg/h) increased mucus gel thickness, induced a hyperemic response to luminal acid, and enhanced pH i homeostasis during acid superfusion. Indomethacin, (5 mg/kg, IP) did not alter the effects of Pentagastrin on acid output, mucus gel thickness, mucosal blood flow, and pH i homeostasis. Indomethacin alone did not affect any of these measures. We conclude that the enhancement of gastric defense mechanisms due to Pentagastrin is independent of prostaglandin synthesis.
Marilla Geraci - One of the best experts on this subject based on the ideXlab platform.
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Pentagastrin induced sleep panic attacks panic in the absence of elevated baseline arousal
Biological Psychiatry, 2002Co-Authors: Marilla Geraci, Robert M Post, Todd S Anderson, Shiyoko Slatecothren, Una D MccannAbstract:Abstract Background It has been suggested that pharmacological challenges that induce panic attacks are confounded by effects of environmental stress, elevated baseline arousal, and expectancy bias. Methods To control for effects of arousal and cognition on the panicogenic effects of Pentagastrin, pharmacological challenges were conducted during sleep in seven patients with panic disorder or social phobia. All patients had previously experienced Pentagastrin-induced panic while awake. Infusions of normal saline and Pentagastrin (0.6 μg/kg) were administered in fixed order and timed so that Pentagastrin infusions took place during the transition from Stage 2 to Stage 3 sleep. Long intravenous lines were placed for remote blood sampling and subsequent analysis of plasma adrenocorticotropic hormone and cortisol. Measures of anxiety and panic were obtained at baseline and upon awakening after pharmacological challenge. Results All seven subjects awoke within seconds following Pentagastrin infusion. Four patients reported symptoms that met criteria for panic. Neither baseline anxiety nor neuroendocrine measures were predictive of panic. Conclusions These data demonstrate the ability to induce panic during a period of diminishing arousal and indicate that panic attacks can occur in the absence of elevated arousal and environmental stress.
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effects of the 5 ht3 antagonist ondansetron on the behavioral and physiological effects of Pentagastrin in patients with panic disorder and social phobia
Neuropsychopharmacology, 1997Co-Authors: Una D Mccann, Christina M Morgan, Marilla Geraci, Shiyoko O Slate, Dennis L Murphy, Robert M PostAbstract:Pentagastrin, a cholecystokinin (CCK) agonist, produces anxiety and panic in patients with panic disorder and social phobia. Preclinical data suggests that Pentagastrin-induced anxiogenesis may be mediated via 5-HT3 receptors. In the present study, 14 patients with panic disorder or social phobia underwent pharmacological challenge in three conditions: (1) pretreatment with saline followed by Pentagastrin infusion; (2) pretreatment with ondansetron followed by Pentagastrin infusion; and (3) pretreatment with saline followed by saline infusion. As expected, Pentagastrin administration led to increased anxiety, physical symptoms of panic attacks, pulse, plasma adrenocorticotropic hormone (ACTH), and cortisol. Pentagastrin's behavioral effects were not blocked by ondansetron, and in fact, tended to be exaggerated. Ondansetron pretreatment did not alter the Pentagastrininduced cortisol increase but significantly prolonged the Pentagastrin-induced increase in ACTH. These findings suggest that Pentagastrin's behavioral effects are not mediated by 5HT3 receptors. Mechanisms by which peripherally administered CCK agonists lead to anxiety remain to be elucidated.
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a comparison of the effects of intravenous Pentagastrin on patients with social phobia panic disorder and healthy controls
Neuropsychopharmacology, 1997Co-Authors: Una D Mccann, Marilla Geraci, Shiyoko O Slate, Diana Roscowterrill, Thomas W UhdeAbstract:The present study sought to determine whether social phobics, like patients with panic disorder, have increased sensitivity to the panicogenic effects of Pentagastrin. Intravenous Pentagastrin and placebo were administered in a double-blind fashion to 19 social phobics, 11 patients with panic disorder, and 19 healthy controls while they participated in a structured social interaction task. Behavioral, cardiovascular, and neuroendocrine responses were obtained. Pentagastrin led to panic attacks in 47% of the social phobics, 64% of the panic disorder patients, and 11% of the healthy controls. The social interaction itself increased anxiety, blood pressure, and pulse in all three groups. These findings suggest that the panicogenic effects of Pentagastrin are not limited to patients with panic disorder and provide further evidence for shared neurobiology in social phobia and panic disorder.
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peptides and anxiety a dose response evaluation of Pentagastrin in healthy volunteers
Anxiety, 1994Co-Authors: Una D Mccann, Marilla Geraci, Shiyoko O Slate, Thomas W UhdeAbstract:A large body of data suggest that brain cholecystokinin (CCK) systems are involved in the regulation of anxiety, and numerous studies have demonstrated that CCK-4, a CCKB agonist, reliably induces panic attacks in patients with panic disorder. Recently, Pentagastrin, a commercially available CCKB agonist, has been reported to have similar anxiogenic properties. To further explore the utility of Pentagastrin as a challenge agent and to determine whether its effects are dose-related, a dose-response study was conducted in ten healthy volunteers. Pentagastrin (0.2 μg kg, 0.6 μg/kg and 1.0 μg/kg) and inactive placebo were infused over one minute on four separate challenge days in a double-blind fashion. Subjects received Pentagastrin while participating in a structured social interaction task. Repeated measures of anxiety, blood pressure, pulse, ACTH, and cortisol were taken at baseline and postinfusion. Pentagastrin administration led to increases in anxiety, pulse, ACTH, cortisol and physical symptoms of panic, in a dose-related manner. Participation in the social interaction task led to increases in measures of anxiety as well as increases in pulse and blood pressure. Few differences were found between the 0.2 μg/kg dose of Pentagastrin and placebo, or between the 0.6 μg/kg and the 1.0 μg/kg doses of Pentagastrin. These findings support the notion that CCK systems are involved in the regulation of anxiety, and suggest that the 0.6 μg/kg dose may be optimal for increasing symptoms of anxiety while minimizing unpleasant side effects. The powerful anxiogenic effects of the social interaction task underscore the importance of contextual variables in challenge studies. Anxiety 1:258–267 (1994/1995). © 1995 Wiley-Liss, Inc.1
Gerard P Smith - One of the best experts on this subject based on the ideXlab platform.
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different effects of cck antagonists on gastric acid response to cck and Pentagastrin
Peptides, 1993Co-Authors: Rebecca L Corwin, Gerard P SmithAbstract:Abstract The role of CCK receptor subtypes in peptide-stimulated acid secretion was assessed in six unanesthetized rats. The CCK-stimulated acid secretion was not blocked by L-365,260, a CCK B /gastrin receptor antagonist, and was significantly increased by devazepide, a CCK A receptor antagonist, give alone or together with L-365,260. L-365,260, but not devazepide, blocked Pentagastrin-stimulated acid secretion, and, when given together, devazepide abolished the effect of L-365,260. We conclude: 1) Pentagastrin stimulates acid secretion through a gastrin-type receptor, but CCK may not, and 2) Pentagastrin and CCK can stimulate acid secretion despite simultaneous blockade of CCK B /gastrin and CCK A receptors.
G Soldani - One of the best experts on this subject based on the ideXlab platform.
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inhibitory effect of the cannabinoid receptor agonist win 55 212 2 on Pentagastrin induced gastric acid secretion in the anaesthetized rat
Naunyn-schmiedebergs Archives of Pharmacology, 1999Co-Authors: G Coruzzi, Maristella Adami, Gabriella Coppelli, Paolo Frati, G SoldaniAbstract:The effect of the cannabinoid (CB) receptor agonist WIN 55,212-2 on gastric acid secretion was studied in the anaesthetized rat after stimulation with Pentagastrin. WIN 55,212-2 (0.5–2 mg/kg, i.v.) was inactive on basal secretion but caused a marked inhibition (80%) of the acid secretion stimulated by Pentagastrin (10 µg/kg, i.v.). The enantiomer WIN 55,212-3 (1–3 mg/kg, i.v.) did not significantly modify basal or Pentagastrin-induced acid secretion. The inhibitory effect of WIN 55,212-2 against Pentagastrin was prevented by the administration of the selective cannabinoid CB1 receptor antagonists SR141716A (1 mg/kg, i.v.) and LY320135 (1 mg/kg, i.v.); by contrast, the CB2 receptor antagonist SR144528 (0.3–1 mg/kg, i.v.) was without effect. The selective CB2 receptor agonist JWH-015 (0.1–10 mg/kg, i.v.) was inactive on the increase of acid output stimulated by Pentagastrin. These results suggest that the inhibitory effect of WIN 55,212-2 on Pentagastrin-stimulated acid secretion in the anaesthetized rat is mediated by specific cannabinoid receptors. Moreover, the antagonism of WIN 55,212-2-induced effects by the selective CB1 receptor antagonists SR141716A and LY320135 together with the ineffectiveness of both the CB2 receptor agonist JWH-015 and the CB2 receptor antagonist SR144528 indicate that CB1 receptor subtypes are predominantly involved in the antisecretory effect of WIN 55,212-2.
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modulation of Pentagastrin induced histamine release by histamine h3 receptors in the dog
Scandinavian Journal of Gastroenterology, 1996Co-Authors: G Soldani, Monique Garbarg, Luigi Intorre, S Bertini, A Rouleau, Jc SchwartzAbstract:Background: The histamine H3 receptor has been shown to inhibit Pentagastrin-induced gastric acid secretion in dogs. Since Pentagastrin releases histamine in dogs, we have now assessed whether the effects of H3-receptor ligands may be indirectly mediated by changes in gastric histamine release. Methods: Pentagastrin infusions (1 or 6 μg/kg/h), alone or together with the H3-receptor agonist (R)α-methylhistamine (1.2 μmol/kg/h) or the antagonist thioperamide (0.1 μmol/kg/h), were performed in dogs. One group (anaesthetized) was used for enzyme immunoassays of plasma histamine and, when required, (R)α-methylhistamine in the gastrosplenic vein, and another group (non-anaesthetized) for measurement of gastric acid secretion. Results: Histamine levels were increased five-and eight-fold after 1 and 6 μg/kg/h Pentagastrin, respectively, whereas acid output was nearly maximal at the lower dosage. (R)α-methylhistamine, at a plasma concentration of 0.15 μM, inhibited histamine release by 78% (P < 0.007) and 37% (not...